PMID- 21345949
OWN - NLM
STAT- MEDLINE
DCOM- 20110620
LR  - 20211020
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Print)
IS  - 0022-538X (Linking)
VI  - 85
IP  - 10
DP  - 2011 May
TI  - TRIM22 inhibits HIV-1 transcription independently of its E3 ubiquitin ligase 
      activity, Tat, and NF-kappaB-responsive long terminal repeat elements.
PG  - 5183-96
LID - 10.1128/JVI.02302-10 [doi]
AB  - Previous studies identified clones of the U937 promonocytic cell line that were 
      either permissive or nonpermissive for human immunodeficiency virus type 1 
      (HIV-1) replication. These clones were investigated further in the search for 
      host restriction factors that could explain their differential capacity to 
      support HIV-1 replication. Among known HIV-1 restriction factors screened, 
      tripartite motif-containing protein 22 (TRIM22) was the only factor 
      constitutively expressed in nonpermissive and absent in permissive U937 cells. 
      Stable TRIM22 knockdown (KD) rescued HIV-1 long-terminal-repeat (LTR)-driven 
      transcription in KD-nonpermissive cells to the levels observed in permissive 
      cells. Conversely, transduction-mediated expression of TRIM22 in permissive cells 
      reduced LTR-driven luciferase expression by  approximately 7-fold, supporting a negative role 
      of TRIM22 in HIV-1 transcription. This finding was further confirmed in the human 
      T cell line A3.01 expressing TRIM22. Moreover, overexpression of TRIM22 in 293T 
      cells significantly impaired basal and phorbol myristate 
      acetate-ionomycin-induced HIV-1 LTR-driven gene expression, whereas inhibition of 
      tumor necrosis factor alpha-induced viral transcription was a consequence of 
      lower basal expression. In agreement, TRIM22 equally inhibited an LTR construct 
      lacking the tandem NF-kappaB binding sites. In addition, TRIM22 did not affect 
      Tat-mediated LTR transactivation. Finally, these effects were independent of 
      TRIM22 E3 ubiquitin-ligase activity. In the context of replication-competent 
      virus, significantly higher levels of HIV-1 production were observed in 
      KD-nonpermissive versus control nonpermissive U937 cells after infection. In 
      contrast, lower peak levels of HIV-1 replication characterized U937 and A3.01 
      cells expressing TRIM22 versus their control transduced counterpart. Thus, 
      nuclear TRIM22 significantly impairs HIV-1 replication, likely by interfering 
      with Tat- and NF-kappaB-independent LTR-driven transcription.
FAU - Kajaste-Rudnitski, Anna
AU  - Kajaste-Rudnitski A
AD  - Viral Pathogens and Biosafety Unit, Division of Immunology, Transplantation, and 
      Infectious Diseases, San Raffaele Scientific Institute, Via Olgettina 58, 20132, 
      Milan, Italy. kajaste.anna@hsr.it
FAU - Marelli, Sara S
AU  - Marelli SS
FAU - Pultrone, Cinzia
AU  - Pultrone C
FAU - Pertel, Thomas
AU  - Pertel T
FAU - Uchil, Pradeep D
AU  - Uchil PD
FAU - Mechti, Nadir
AU  - Mechti N
FAU - Mothes, Walther
AU  - Mothes W
FAU - Poli, Guido
AU  - Poli G
FAU - Luban, Jeremy
AU  - Luban J
FAU - Vicenzi, Elisa
AU  - Vicenzi E
LA  - eng
GR  - R21 AI087467/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110223
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (Minor Histocompatibility Antigens)
RN  - 0 (Repressor Proteins)
RN  - 0 (TRIM22 protein, human)
RN  - 0 (Tripartite Motif Proteins)
SB  - IM
MH  - Cell Line
MH  - HIV-1/*growth & development/*immunology
MH  - Humans
MH  - Minor Histocompatibility Antigens
MH  - Monocytes/immunology/virology
MH  - Repressor Proteins/*metabolism
MH  - T-Lymphocytes/immunology/virology
MH  - *Transcription, Genetic
MH  - Tripartite Motif Proteins
MH  - *Virus Replication
PMC - PMC3126207
EDAT- 2011/02/25 06:00
MHDA- 2011/06/21 06:00
PMCR- 2011/11/01
CRDT- 2011/02/25 06:00
PHST- 2011/02/25 06:00 [entrez]
PHST- 2011/02/25 06:00 [pubmed]
PHST- 2011/06/21 06:00 [medline]
PHST- 2011/11/01 00:00 [pmc-release]
AID - JVI.02302-10 [pii]
AID - 2302-10 [pii]
AID - 10.1128/JVI.02302-10 [doi]
PST - ppublish
SO  - J Virol. 2011 May;85(10):5183-96. doi: 10.1128/JVI.02302-10. Epub 2011 Feb 23.